Unit 3 - Motor Control Flashcards
(71 cards)
0
Q
Lower motor neurons
A
Motor neuron projecting from spinal cord to the motor end plate on muscle,
Synapses with upper motor neuron in ventral horn
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Q
Upper motor neuron
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Projects from cortical areas to spinal cord, synapses with lower motor neuron
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Q
Higher cortical areas
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–> no direct contact with spinal cord, so influence = indirect.
ie: association cortex, basal ganglia, and cerebellum
(Signal via thalamus)
3
Q
Spinal circuit reflex
A
Most simple motor circuit,
Sensory receptors –> spinal grey matter –> muscle
(Cutaneous, pain or muscle spindles)
ie: stretch reflex
4
Q
Central pattern generator (CPG)
A
Moderately complex motor circuit;
Generated at brainstem or spinal cord,
INdependent of descending input, but turned on/off by cortex
Ex: walking or breathing
5
Q
ballistic movement
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rapid movement that MUST go to completion
(can’t withdraw action once started)
ie: saccades (eyes), hemiballismus
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Q
organization of motor neurons in spinal cord
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Medial: axial muscles – control balance/stability
Lateral: distal muscles – fine motor control
dorsal: flexor mm.
ventral: extensor, mm.
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Q
motor unit
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a single alpha motor neuron, along with all muscle fibers innervated by it (3-1,000)
- small size = fine motor control
- increase muscle force by recruiting motor units
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Q
2 types of alpha motor neurons (+ function)
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“red” (small): slow, low force, fatigue-resistant
“pale” (large): fast, fatiguable
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Q
monosynaptic/myotactic reflex
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- passive stretch of tendon
- a) contract muscle (via muscle spindle Rs)
b) relax opposing muscle (“reciprocal inhibition”)
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Q
nocioceptive withdrawal reflex
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1. nocioRs sense pain (ie: step on tack)
(--> Lissauer's tract)
2. a) ipsilateral flexor contracts
b) contralateral extensor contracts
* provides support for opp. limb to "escape"
11
Q
Muscle proprioceptive pathway
A
- muscle spindle (stretch R)
- ipsilateral dorsal column - spinal cord
- dorsal column nucleus
* decussate!* - contralateral medial lemmniscus
- VPL of thalamus –> S1 (cortex)
12
Q
muscle spindle
A
in parallel with mm., w/ stretch Rs;
- -> passive stretch/increase muscle length
- 1a and II axons
- gamma mns change length to increase sensitivity (via intrafusal fibers)
- stimulated by vibration (lengthening illusion)*
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Q
Golgi tendon
A
in series w/ mm (at end, inside collagen);
- -> isometric contraction (tension on muscle)
- 1b axons to inhib. interneurons, compensate for fatigue
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Q
Lesion to posterior parietal cortex
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- apraxia (loss of learned/skilled movements)
2. optic ataxia (mis-reaching)
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Q
Lesion to premotor/supplementary motor cortex
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poor planning and sequencing,
decreased spatial organization
* feet = medial, head = lateral
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Q
lesion to basal ganglia
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- akinesia/bradykinesia (slowed mvmt)
- ballismus
(responsible for selection and initiation of mvmt)
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Q
lesion to cerebellum
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ataxia (uncoordinated mvmt)
* normally responsible for mvmt smoothness and coordination
18
Q
Cortical circuits involved in voluntary movement
A
Direct to spinal neurons:
1. corticospinal tract; 2. corticobulbar (*bilateral!)
INdirect to spinal neurons:
1. corticorubral tract; 2. corticoreticular tract
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Q
Thalamic motor control
A
- VPL = somatosensory (proprioceptive/cutaneous info)
2. VA/VL = timing/coordination
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Q
Major cortical motor areas
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1.Primary motor cortex (BA 8)
2. Supplementary motor cortex (BA 6)
3. Premotor cortex (BA 6)
4. Cingulate Motor area (BA 24)
Req’s: thin granular layer (IV), & electrical stim. to area –> mvmt
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Q
Neurons in primary motor cortex (M1)
A
each = directionally tuned,
fire: just before & during mvmt, (latency = 100-150 ms)
* population vector of neurons matches direction of mvmt*
- - increase firing rate = increase force
22
Q
lesion to pyramidal tract
A
decrease in hand control, ie:
- thumb-finger opposition
- precise grip (=> “scoop hand”)
- single digit extension
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Q
lesion to primary motor cortex
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- -> spastic paresis (bc = upper motor neurons)
- lose fine motor control
- increase tone/hyper-reflexia
- adjacent representations fill in void! (modified by use/experience)
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Function of Premotor cortex (BA 6)
#1) learned visual stimulus-response associations
2) rule-based actions
3) motor planning (to instructional cue)
* ventral (PMv) = hand grasp & mirror neurons
* dorsal (PMd) = arm reach
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Supplementary motor area function (SMA):
self-initiated mvmts, mental mvmt rehearsal, and learned motor sequences.
* single neurons = selective for specific mvmt sequences (Bop-it);
- -- "bereitshift potential" = from EEG over SMA.
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"distributed processing" for motor cortex:
Multiple distinct cortical areas responsible for motor processing,
* all areas have different but overlapping function*
--> damage to 1 area = mild/transient,
BUT damage to >1 area = severe, persistant
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input to inferior cerebellar peduncle:
1. vestibular nuclei
2. brainstem
3. spinal cord
* output = vestibular nuclei
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input to Middle Cerebellar Peduncle:
1. Pontine Relay Nuclei
2. Cerebral cortex
(output = cerebellum)
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Cellular organization of the cerebellum
3 layers, 5 total cell types.
1. Purkinje layer: 1 cell thick (purkinje cell bodies)
2. Molecular layer: purkinje dendrites, parallel fibers, and interneurons
3. Granular layer: granule cells (= cell bodies of parallel fibers),
* inhibited by Golgi cells (interneurons, NT = GABA)
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synapses on Purkinje cells
all use glutamate as excitatory NT,
1. Climbing fibers (from Inf. Olive) --> short AP burst
= motor error signal (teaching)
2. Granule cells (become parallel fibers) --> single AP
= sensory feedback/motor commands
*** Purkinje cells = INhibitory to Deep Cerebellar Nuclei ***
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Climbing fibers
neurons connecting Inferior Olive to Purkinje Cells (excitatory),
for signaling motor errors;
input to Inf.O. from:
Cerebral cortex, Red Nucl., Spinal Cord, Deep Cerebellar Nuclei
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Mossy Fibers
neurons in cerebellum connecting input to Purkinje cells (excit.),
via Granule cells/parallel fibers.
Input from: Cerebral cortex, Brainstem and Spinal cord.
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Long-term Depression
phenomenon where parallel fiber signaling is weakened by simultaneous firing of climbing fibers.
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Output from cerebellum
info from cerebellum to a) motor thalamus, b) Red Nucleus
| via Superior Cerebellar Peduncle.
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Inferior Olive (relation to cerebellum)
Receives input from Cortex, Red Nucleus, Spinal Cord, and Deep Cerebellar Nuclei ("Loop Circuit").
* sends to CONTRAlateral cerebellar hemisphere.
Inferior Olive --> Climbing Fibers --> Purkinje Cell(s)
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unilateral lesions in cerebellum cause...
Hypotonia (if decrease gamma motor neuron activity via thalamus),
= IPsilateral deficits bc cross twice (in SCP and after M1)
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Vestibulocerebellum
= vermis and flocculonodular lobe.
controls balance and eye mvmts,
Inputs: vestibular nuclei, visual cortex, motor cortex (for posture)
Output: Vestibular nucleus
Lesion deficits:
- balance: fall to side of lesion,
- Eyes: spontaneous nystagmus, poor smooth pursuit (eyes(
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Spinocerebellum
= vermis and medial hemispheres;
Receives somatosensory info.
Input: spinal cord (ipsilateral limb tracts)
Output: to Reticular Formation (via Fastigial nucleus)
Lesion Deficits:
Ataxia, dysmetria (poor coordination), hypotonia, tremor, poor rapid alt. mvmts/decomposed mvmt.
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Cerebrocerebellum
= lateral hemisphere; helps w/ voluntary mvmt.
Input: Motor cortex, somatosensory cortex, Association cortex
Output: Motor thalamus (via dentate nucleus)
Lesion Deficits: fine mvmt ataxia, cognitive deficits
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Basal Ganglia
"Gates" mvmt (selection and initiation); somatotopic organization.
= Striatum, Globus Pallidus, Subthalamic nucl, and Substancia Nigra.
-- Direct Path: suppress inhibition --> increase motor output.
--- Indirect: inhibit direct path --> decrease motor output.
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lesion to caudate nucleus
deficit = robotic walking
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Lesion to putamen
deficit = vulgar and impulsive personality shift, hypersexuality
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striatum neurons
= medium spiny neurons ("MSNs") --> inhibitory projections to globus pallidus, NT = GABA.
(+ some interneurons)
* somatotopic organization
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Nigrostriatal pathway
from STN (subthalamic nucleus) to Striatum;
D1 Rs: + to MSNs in Direct path.
D2 Rs: - to MSNs in INdirect path
==> promote movement (aka motor output)
** Dopamine deficit in Parkinson's limits this pathway.
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Parkinson's Disease
--> akinesia, bradykinesia, slow rest tremor
= Dopamine deficit to nigrostriatal pathway,
From oxidative stress, mimicked by MTPT drug.
Treatment: L-DOPA, Pallidotomy (decrease inhibitory GPi output), DeepBrain Stimulation
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Huntington's Disease
autosomal dominant mutation (CAG repeat on chrom.4 short arm)
-> MSNs and cerebral cortical neurons die
==> chorea, athetosis (slow writing), Dementia, and personality changes.
* 30-50 yr. onset
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Direct Basal ganglia pathway
Cortex --> (+) striatum --I (-) GPi/SNr -/-I Thalamus
| ==> suppress inhibition = increase motor output
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INdirect Basal Ganglia pathway
Cortex--> striatum--I GPe -/-I (-)STN --> (+)GPi/SNr --I Thalamus
==> inhibit direct pathway = Decrease motor output
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Lesion to Globus pallidus
--> dystonia (sustained muscle contractions, abnormal postures, etc.)
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lesion to Subthalamic Nucleus (STN)
--> hemiballismus (involuntary flinging motion in extremities)
bc lesion causes LOSS in mvmt inhibition (via INdirect pathway)
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Muscle groups used for postural tone
(tonic activity in muscles opposing gravity)
- Upper limb flexors
- Lower limb extensors
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2 routes for postural control
1. Direct: via vestibulospinal tract to alpha mns
2. Reflex Route: via corticospinal or reticulospinal tracts to gamma mns
==> act on muscle spindles to increase tone via alpha mns
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Reticulospinal tract and postural control:
to modulate gamma mns --> affect alpha mns;
a) Cortex --I Pontine Reticular Formation --> + gamma mns
= increase m. tone.
b) Cortex --> Medullary Reticular Formation --I - gamma mns
= DEcrease tone.
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Lesion to "MRF" (medullary reticular formation):
INcreased tone bc DISinhibit gamma neurons
| (so increase alpha mn work too)
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Median Vestibular tract ("MST")
carries bilateral cervical information from semicircular ducts,
=> stabilize head position, influence alpha mns to neck muscles.
(maintain center of gravity)
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Lateral Vestibular tract (LVST)
ipsilateral to all levels of spinal cord,
=> stabilize stance/maintain balance and posture.
to alpha mns of legs
(anti-gravity and tilt reflexes)
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Lesion to vestibulospinal tracts
loss of balance,
| will fall towards side of lesion
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Decortication
lesion above the red nucleus, so red nuc = DISinhibited;
(ie: cerebral cortex, internal capsule, thalamus)
Sx --> flex arms and extend legs
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decerebration
lesion below the red nucleus, disrupts the rubrospinal tract
(loss of tonic input from cortex --> hyperactive stretch reflex)
-> increase gamma mn activity = increase postural tone
Sx --> extend arms and legs, arch head back
Treatment: cut dorsal roots to decrease rigidity
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Reasons for return of sensation >2 months after lesion
| to descending systems
- -> hyperactive reflexes and hypertonic bc...
1. denervation sensitivity (increase sensitivity to input)
2. synaptic void filled by nearby neurons (increase strength of proximal circuits)
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saccade
ballistic mvmt to rapidly redirect fovea,
*not modifiable once started, = CPG reflex.
** CAN perform on verbal command**
During mvmt: blurry image and no f(x)al vision
Latency: 150-200 ms, Duration: 20-50 ms
Velocity: ~400 degrees/second
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Smooth pursuit (eye mvmt)
eye mvmt to follow moving target -- eyes match speed of target;
*"retinal slip" = speed mismatch
* canNOT perform on visual command (uses saccadic tracking)*
DO have f(x)al vision while move eyes
= voluntary cortical modulation of reflex mech in brainstem
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Lesion to cortical eye fields and/or brainstem visual centers
1 or other: mild, transient saccade deficits
Both areas: severe and persistent saccade deficits
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Cortical eye fields
code direction and amplitude of eye movement,
each neuron = directionally tuned.
= frontal/supplementary eye fields and lateral intraparietal area;
*project to: a) brainstem (saccade reflex)
b) pontine relay nuclei/cerebellum (smooth pursuit)
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Superior colliculus
1 of 2 visual centers in brainstem, = on tectum of midbrain;
F(x): reflexive, contralateral saccades
- superficial layer: stimulus position
- deep layer: direction/amplitude of saccade
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reticular formation
```
1 of 2 visual centers in brainstem,
= saccade central pattern generator
a) midbrain (riMLF) = vertical component
- output: abducens nucleus
b) pons (PPRF) = horizontal component
- output: occulomotor nucleus
*output goes 1st to nucleus of IPsilateral eye!
```
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"Pulse-step" pattern for visual saccades
= firing pattern in abducens and occulomotor nuclei;
1. pulse: burst --> saccade
2. step: tonic activity --> fixation/tension
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pathway for smooth pursuit:
1. cortical eye fields/extrastriate visual cortex
- via Pontine Relay Nuclei -
2. Cerebellum: Flocculum
3. Vestibular nuclei
4. Brainstem nuclei (direct to abducens, INdirect to occulomotor)
5. Eye muscles
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Function of Vermis (cerebellum) in saccades
adjusts amplitude of saccade to match target
(so gaze lands accurately on target)
*Lesion ==> dysmetric saccades (miss/overshoot target)
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Lesion to flocculum (cerebellum)
--> smooth pursuit = abolished!
but saccades not affected.
(so use saccadic tracking to overcome deficit)
